Faivre-Sarrailh C, Clavel M C, Rabié A
Laboratoire de Neurobiologie Endocrinologique, URA 1197 CNRS, Université Montpellier II, France.
Dev Neurosci. 1991;13(2):80-6. doi: 10.1159/000112198.
The immunocytochemical staining of tyrosylated alpha-tubulin using the specific monoclonal antibody YL 1/2 decreases dramatically in the parallel fibers of the rat cerebellum during development. Detyrosylation starts at 14 days in the deeper part of the molecular layer and then spreads over the entire molecular layer within a week. Thyroid deficiency induces a marked delay in alpha-tubulin detyrosylation in the parallel fibers. Detyrosylation begins only at the age of 28 days in hypothyroid animals. Immunobinding assays of detyrosylated and tyrosylated alpha-tubulin concentrations in the cerebellar supernatant of developing rats confirm that thyroid deficiency increases the tyrosylated alpha-tubulin content at 21 and 35 days. Short-term thyroxine treatment (daily from day 8, 10 or 12, to day 14) do not induce the normal pattern of tubulin detyrosylation starting at 14 days, although they do induce parallel fiber lengthening. Daily treatment from birth is required to produce the alpha-tubulin modification found in normal rats. We propose that the microtubule detyrosylation which occurs during axonal maturation is not a prerequisite for axon growth and synaptic differentiation, but may rather be implicated in the stabilization of microtubules in the mature axons.
使用特异性单克隆抗体YL 1/2对酪氨酸化α-微管蛋白进行免疫细胞化学染色，结果显示，在大鼠小脑发育过程中，平行纤维中的染色显著减少。去酪氨酸化始于分子层深部的14天，然后在一周内扩展至整个分子层。甲状腺功能减退会导致平行纤维中α-微管蛋白去酪氨酸化明显延迟。在甲状腺功能减退的动物中，去酪氨酸化仅在28日龄时开始。对发育中小鼠小脑上清液中去酪氨酸化和酪氨酸化α-微管蛋白浓度进行免疫结合分析证实，甲状腺功能减退会使21日龄和35日龄时酪氨酸化α-微管蛋白含量增加。短期甲状腺素治疗（从第8、10或12天开始每日给药，直至第14天）虽然会诱导平行纤维延长，但不会诱导从14天开始的正常微管蛋白去酪氨酸化模式。需要从出生开始每日给药才能产生正常大鼠中发现的α-微管蛋白修饰。我们提出，轴突成熟过程中发生的微管去酪氨酸化不是轴突生长和突触分化的先决条件，而可能与成熟轴突中微管的稳定有关。
